What do the results show?
Wild type or “normal” worms habituate after 6-7 touches to both the head and tail. This result serves as our standard in understanding the role of apl-1 in worm learning behaviors. If we observe that the rate of learning for the “normal” worms is 6-7 touches, then we may attribute differing learning rates of genetically different worms to their genetic makeup. The apl-1(yn5) worms habituate after approximately 5 touches, which is faster than the wild-type worms. In another study, researchers found that when apl-1 is pan-neuronally expressed, even more repeated stimuli was needed to touch habituate (Ewald et al, 2012). This shows that the apl-1 gene disrupts normal learning behavior.
Based on these results, there appears to be a converse relationship between the apl-1(yn5) mutant and wild-type worms. Worms with more truncated apl-1 fragments appear to be learning at a faster rate than the normal worms. And the reasoning behind this trend remains unclear! It is possible that apl-1 is interacting with other genes to create this trend. It is also possible that the learning behavior can be influenced by many other molecular pathways. Further study is definitely needed!
This research does not translate directly to human learning behavior in patients with Alzheimer’s disease. Rather it serves as a model for a preliminary understanding of the molecular mechanisms underlying learning and how it is impacted and influenced by the apl-1 gene in worms. We can only infer its application to the APP gene in humans. Current studies show that more APP fragments are found in the (human) brains of Alzheimer’s disease patients post-mortem and that with increased levels of apl-1 in worms, habituation rates increase. Taken together, we may infer that there is a relationship between the increased presence of APP fragments and a decline in cognitive function.
Different organisms may share common genes, but it does not necessarily mean that those genes will manifest themselves in the same way in those organisms. So while the worms may share an evolutionarily common gene with humans, they do not have the plaques, tangles, or Alzheimer’s disease that the human form of the gene dictates. Instead the worms provide a much simpler model to study the complexities of this human disease. And it is my hope that by writing and drawing out this simplified explanation, I have attempted to breakdown the intricacies of the research being done to enhance our collective understanding of Alzheimer’s disease.
